Transmembrane signals generated through MHC class II, CD19, CD20, CD39, and CD40 antigens induce LFA-1-dependent and independent adhesion in human B cells through a tyrosine kinase-dependent pathway.

Transmembrane signals generated following mAb binding to CD19, CD20, CD39, CD40, CD43, Leu-13 Ag, and HLA-D region gene products induced rapid and strong homotypic adhesion in a panel of human B cell lines. Lower levels of adhesion were also observed after engagement of CD21, CD22, and CD23. Adhesion induced by mAb binding to these Ag was identical with respect to the kinetics of adhesion and the morphology of the resulting cellular aggregates, and was distinct from PMA-induced adhesion in both of these properties. Adhesion was not observed in response to mAb binding to MHC class I, CD24, CD38, CD44, CD45RA, or CD72. In contrast to B cell lines, homotypic adhesion was not induced in two pre-B cell lines, in spite of their high level expression of CD19 and HLA-D. Adhesion induced by suboptimal stimulation through these surface Ag or by PMA was mediated primarily through LFA-1 and ICAM-1. However, optimal stimulation through CD19, CD20, CD39, CD40, and HLA-D induced strong homotypic adhesion that was not blocked by anti-LFA-1 mAb. This alternate pathway of adhesion was also observed in LFA-1-deficient cell lines and in the presence of EDTA, suggesting that adhesion was not mediated by integrins. Adhesion in response to engagement of cell-surface Ag was unaffected by H7 or genestein, but was significantly inhibited by staurosporine, and was completely ablated by sphingosine and herbimycin. These studies indicate that engagement of multiple B cell-surface molecules initiates a signal transduction cascade that involves tyrosine kinases but not protein kinase C, and which leads to homotypic adhesion. Furthermore, adhesion was mediated by at least two distinct cell-surface adhesion receptors: LFA-1/ICAM-1 and a heretofore unknown adhesion receptor.     

牛疱疹病毒Ⅳ型(DN-599株)DNA的限制性酶切位点图及重复序列分析

牛疱疹病毒Ⅳ型(BHV-4)DNA片段分别被重组到质粒pUC9或pBR322的EcoRI、Hind Ⅲ和BamHⅠ位点中,用光生物素(Photobiotin)标记这些重组质粒作为探针,分别与转移到硝基纤维素膜上的病毒DNA的EcoRⅠ、Hind Ⅲ和BamHⅠ片段进行杂交,根据杂交结果及克隆的BHV-4DNA片段的双酶切分析,画出了病毒DNA的EcoRⅠ、Hind Ⅲ和BamHⅠ位点图,井证明在病毒DNA的两末端含有多聚重复序列,左侧含12个重复单位,右侧含6个重复单位,两侧重复单位的排列方向相同,重复单位的大小为2.35kb。病毒DNA分子无任何异构体.     

Expression of adhesion structures during B cell development in man

We have used three-color flow cytometry to study the expression of adhesion structures during B cell development in man. The results indicate that the cell-surface molecule(s) recognized by 515, a mAb which defines a broadly expressed family of cell-surface glycoproteins that includes lymphocyte homing receptors, exhibit a clear bimodal distribution (515lo and 515hi); 515hi cells were found exclusively on more mature B cells which already expressed high levels of CD20. Earlier, less mature B cells, identified by their expression of CD10, were uniformly 515lo. In contrast, the CD11a/LFA-1 Ag was acquired gradually over the course of B cell development. B cells which expressed high levels of CD20 expressed three to six times as much CD11a/LFA-1 as cells which expressed CD10. Interestingly, expression of the 515hi phenotype was tightly correlated with that of Leu-8, a marker previously shown to define maturational and functions subsets of B cells. These data document the coordinated regulation of multiple cell surface structures during B cell ontogeny, and demonstrate that adhesion structures necessary for proper B cell function are precisely up-regulated during B cell differentiation in man.     

上海3个公园园林小气候的人体舒适度测析

小气候影响着公共空间的使用率和使用频度,人体舒适是园林规划设计追求的一个重要目标,然而现代景观实践缺乏气候敏感性设计和关于人体舒适度的考虑。本文以上海3个公园为例,采取“使用后评价”并结合描述性分析的方法来测试人体舒适度。通过硬质景观和软质景观面积比、绿化覆盖率差异、近水面积比及日照空间比等对公园空间进行分类。在对公园使用者进行调查的基础上,对每个公园小气候特征进行测量以量化人体舒适度,研究发现,通过小气候设计可以创造更多的人体舒适空间。     

Microhabitat use by white-footed mice Peromyscus leucopus in forested and old-field habitats occupied by Morrow's honeysuckle Lonicera morrowii

We quantified microhabitat use by white-footed mice Peromyscus leucopus in forest and old-field habitats occupied by Morrow's honeysuckle Lonicera morrowii, an invasive exotic shrub imported from Japan. Microhabitat characteristics were compared between trails used by mice (n=124) and randomly selected trails (n=127) in 4 study plots located at Fort Necessity National Battlefield, Farmington, Pennsylvania, USA. We compared 10 microhabitat variables between used and random trails using non-metric multidimensional scaling (NMDS) and classification and regression tree (CART) analysis. Trails used by mice were statistically different from randomly selected trails in both forested plots (P<0.008) and old-field plots (P<0.001). In the forested plots, trails of white-footed mice were more often associated with a greater percent cover (% cover) of coarse woody debris (CWD) than were randomly selected trails. In the old-field plots, mouse trails were commonly characterized by having a lower % cover of exotic herbaceous vegetation, a greater % cover of shrubs, and a greater % cover of Morrow's honeysuckle than randomly selected trails. Our study indicates that white-footed mice do not move randomly and prefer areas of high structural complexity, thereby showing significant microhabitat preference. The preference of white-footed mice for areas with a relatively high percent cover of Morrow's honeysuckle could 1) be a factor in the aggressive nature of the exotic honeysuckle shrub's spread throughout the Battlefield or 2) cause the shrub to spread even faster into adjacent areas not yet occupied by Morrow's honeysuckle[Current Zoology 55(2):111-122,2009].     

表达H5N1亚型禽流感病毒HA蛋白的重组鼠白血病病毒的特性

通过反转录 聚合酶链式反应 (RT PCR)扩增了H5N1亚型鹅源禽流感病毒 (AIV)完整的血凝素 (HA)基因并进行了克隆与鉴定。序列测定结果已经登陆GenBank ,登陆号为AY6 394 0 5。序列分析表明所扩增的HA基因开放性阅读框架 (ORF)由170 7个核苷酸组成 ,共编码 5 6 8个氨基酸 ,裂解位点的氨基酸组成为RKKR↓GLF ,含连续的碱性氨基酸 ,具有高致病性AIVHA基因裂解位点的特征。构建了含HA基因的真核表达载体pcDNA HA ,通过与鼠白血病病毒 (MuLV)假病毒构建体系的两种质粒pHIT6 0和pHIT111共转染人胚肾细胞 2 93T ,4 8h后收集假病毒上清 ,超离后通过Western blot证明HA蛋白能够在假病毒颗粒表面表达 ,表明HA能够整合到此病毒粒子表面。通过感染 2 93T、COS 7和NIH3T3三种不同的靶细胞 ,证实所构建的假病毒粒子具有感染性和泛嗜性。本研究成功构建了具有感染性的MuLV HA假病毒体系 ,为研究鹅源禽流感病毒侵入细胞的机理及其组织嗜性的变异提供一种新方法。     

绿脓杆菌pprA与pprB基因的克隆及其抗药性研究

从绿脓杆菌(Pseudomonas aeruginosa)PAK菌株的染色体DNA构建的基因文库中筛选到一 基因片段与绿脓杆菌的抗性相关。经测序证明该片段包含了绿脓杆菌基因组中PA4293所编码 序列,进一步实验证明与它相邻的另一段827bp的基因也与绿脓杆菌的抗药性有关。上述2基 因分别命名为pprA和pprB。以绿脓杆菌PAK菌株为出发菌株,经过新霉素耐受培养得到抗生素 抗性菌株PAK1-3,该菌株对氨基糖苷类抗生素的抗性明显增强。经PCR方法扩增上述基因并克 隆至PAK1-3菌株中,可引起该菌株对氨基糖苷类抗生素的敏感。又经pprB基因转入临床分离 得到的致病性绿脓杆菌中,导致部分绿脓杆菌对氨基糖苷类抗生素的敏感性增强。pprA和pprB 很可能是一组与绿脓杆菌抗药性相关的双分子调节系统,并与细胞膜的通透性有关。     

Chinese NGOs in action against HIV/AIDS

INTRODUCTION The AIDS epidemic continues its seemingly inexorable spread throughout the world. It is now very clear that the virus represents not only a medical problem, but also a challenging and multifaceted social problem. Because of this fact, it is imperative that nongovernmental organiza- tions outside of, or tangential to, the medical arena be- come involved in prevention and control efforts. The Chinese government is supportive of the development of such organizations on the mai…     

Cytoplasmic anchorage of L-selectin controls leukocyte capture and rolling by increasing the mechanical stability of the selectin tether

L-selectin is a leukocyte lectin that mediates leukocyte capture and rolling in the vasculature. The cytoplasmic domain of L-selectin has been shown to regulate leukocyte rolling. In this study, the regulatory mechanisms by which this domain controls L-selectin adhesiveness were investigated. We report that an L-selectin mutant generated by truncation of the COOH-terminal 11 residues of L-selectin tail, which impairs association with the cytoskeletal protein alpha-actinin, could capture leukocytes to glycoprotein L-selectin ligands under physiological shear flow. However, the conversion of initial tethers into rolling was impaired by this partial tail truncation, and was completely abolished by a further four-residue truncation of the L-selectin tail. Physical anchorage of both cell-free tail-truncated mutants within a substrate fully rescued their adhesive deficiencies. Microkinetic analysis of full-length and truncated L-selectin-mediated rolling at millisecond temporal resolution suggests that the lifetime of unstressed L-selectin tethers is unaffected by cytoplasmic tail truncation. However, cytoskeletal anchorage of L-selectin stabilizes the selectin tether by reducing the sensitivity of its dissociation rate to increasing shear forces. Low force sensitivity (reactive compliance) of tether lifetime is crucial for selectins to mediate leukocyte rolling under physiological shear stresses. This is the first demonstration that reduced reactive compliance of L-selectin tethers is regulated by cytoskeletal anchorage, in addition to intrinsic mechanical properties of the selectin-carbohydrate bond.     

Potent induction of alpha(1,3)-fucosyltransferase VII in activated CD4+ T cells by TGF-beta 1 through a p38 mitogen-activated protein kinase-dependent pathway

Homing of effector T cells to sites of inflammation, particularly in the skin, is dependent on T cell expression of ligands for the endothelial selectins. Underlying expression of these ligands is the expression of alpha(1,3)-fucosyltransferase VII (FucT-VII), a FucT essential for biosynthesis of selectin ligands. FucT-VII is sharply induced in activated T cells by IL-12, but cytokines other than IL-12 that induce FucT-VII and functional selectin ligands have not been identified, and are likely to be important in homing of T cells to other selectin-dependent sites. Screening of a number of cytokines known to be active on T cells identified only TGF-beta1 as able to up-regulate FucT-VII mRNA levels and selectin ligands on activated CD4 T cells. The sharp increase in FucT-VII induced by TGF-beta1 in activated T cells was completely blocked by pharmacologic inhibition of p38 mitogen-activated protein kinase, but was unaffected by mitogen-activated protein/extracellular signal-related kinase kinase inhibitors. The selective ability of TGF-beta1 to induce selectin ligands on activated T cells is likely important for T cell homing to the gut, which is a strongly selectin-dependent site, and correlates with the ability of TGF-beta1 to coordinately induce other gut-associated homing pathways.